RGD Reference Report - Spironolactone reversed hepato-ovarian triglyceride accumulation caused by letrozole-induced polycystic ovarian syndrome: tissue uric acid-a familiar foe. - Rat Genome Database

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Spironolactone reversed hepato-ovarian triglyceride accumulation caused by letrozole-induced polycystic ovarian syndrome: tissue uric acid-a familiar foe.

Authors: Adeyanju, Oluwaseun A  Falodun, Timothy O  Michael, Olugbenga S  Soetan, Olaniyi A  Oyewole, Aboyeji L  Agbana, Richard D 
Citation: Adeyanju OA, etal., Naunyn Schmiedebergs Arch Pharmacol. 2020 Jun;393(6):1055-1066. doi: 10.1007/s00210-020-01809-1. Epub 2020 Jan 10.
RGD ID: 401976287
Pubmed: PMID:31925474   (View Abstract at PubMed)
DOI: DOI:10.1007/s00210-020-01809-1   (Journal Full-text)

Polycystic ovarian syndrome (PCOS) is a complex endocrine disease among women of reproductive age and is one of the main causes of infertility. Non-alcoholic fatty liver disease (NAFLD), the most prominent chronic liver disease in adults, is characterized by excess hepatic triglyceride (TG) accumulation. PCOS women have increased risk of NAFLD and uric acid has been documented to have a positive correlation with subclinical tissue damage and might be the link in the cystic. Spironolactone (SPL) is a mineralocorticoid receptor (MR) blocker that has been in wide clinical use for some decades. In this research, we investigated the effects of SPL on ovarian and hepatic tissue damage in experimental PCOS rats induced by letrozole (LET). A total of eighteen adult female Wistar rats were used for this study and the animals divided into 3 groups are treated with vehicle, LET (1 mg/kg), and LET+SPL (SPL; 0.25 mg/kg), p.o. once daily respectively for 21 uninterrupted days. Results showed that LET treatment induced features of PCOS characterized by increased plasma testosterone (T) and luteinizing hormone (LH) together with increased body weight. Abnormal ovarian and hepatic histomorphological changes were also observed with elevated uric acid (UA) and TG accumulation in both tissues respectively. Treatment with SPL however attenuated the elevated testosterone in the LET-induced PCOS model accompanied with a reversal in the observed ovarian and hepatic UA, TG accumulation, and altered histomorphological changes. Taken together, spironolactone reversed the PCOS-induced ovarian and hepatic tissue damage by suppressing tissue UA and TG accumulation.



RGD Manual Disease Annotations    Click to see Annotation Detail View
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
NR3C2Humanpolycystic ovary syndrome treatmentISONr3c2 (Rattus norvegicus) RGD 
Nr3c2Ratpolycystic ovary syndrome treatmentIMP  RGD 
Nr3c2Mousepolycystic ovary syndrome treatmentISONr3c2 (Rattus norvegicus) RGD 

Objects Annotated

Genes (Rattus norvegicus)
Nr3c2  (nuclear receptor subfamily 3, group C, member 2)

Genes (Mus musculus)
Nr3c2  (nuclear receptor subfamily 3, group C, member 2)

Genes (Homo sapiens)
NR3C2  (nuclear receptor subfamily 3 group C member 2)


Additional Information